XB-ART-18379
J Neurobiol
1996 Apr 01;294:415-28. doi: 10.1002/(SICI)1097-4695(199604)29:4<415::AID-NEU1>3.0.CO;2-B.
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Exogenous nitric oxide causes collapse of retinal ganglion cell axonal growth cones in vitro.
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We show that nitric oxide (NO) from applied NO-donating chemicals induces collapse of ganglion cell axonal growth cones extending from explants of tadpole retina in culture. Peroxynitrite, a neurotoxic product of NO and superoxide reaction, did not induce collapse, and oxyhemoglobin, which binds NO, blocked the highly effective collapsing activity of the NO donor S-nitrosocysteine. Membrane-permeable analogs of cyclic guanosine monophosphate had no collapsing activity. Inhibitors of NO synthase did not induce collapse. NO is a potential retrograde messenger through which postsynaptic neurons signal to their inputs to modify synaptic efficacy following NMDA receptor activation. Our results suggest a role for NO as such a messenger during development of the retinotectal projection.
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